Direct comparison of the dynamics of <scp>IL</scp>‐25‐ and ‘allergen’‐induced airways inflammation, remodelling and hypersensitivity in a murine asthma model

Yao, Xiujuan; Huang, Kewu; Li, Y.; Zhang, Q.; Wang, J. J.; Wang, W.; Liu, J.; Lv, Zhe; An, Yongbo; Ding, Yi-Tao; Corrigan, Christopher; Ying, Sun

doi:10.1111/cea.12298

Cited by 38 publications

(80 citation statements)

References 42 publications

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“…To compare the differences between IL‐33‐induced and IL‐25‐induced airway changes, mice were randomly distributed into four groups including a group serially challenged with 50 μg/dose of OVA as a positive control, a group administered saline as a negative control, a group serially challenged with IL‐25 and a group serially challenged with IL‐33 . In brief, mice challenged with OVA were first sensitized by intraperitoneal injection of 100 μg/dose OVA (Sigma‐Aldrich, Beijing, China, emulsified in Al[OH] 3 ) on days 0 and 12 . These mice were then further challenged daily intranasally on days 18 to 23 with 50 μg/dose of OVA (OVA 50 ) in 50 μl saline.…”

Section: Methodsmentioning

confidence: 99%

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Distinct sustained structural and functional effects of interleukin‐33 and interleukin‐25 on the airways in a murine asthma surrogate

Wang

Huang

et al. 2015

Immunology

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SummaryInterleukin-25 (IL-25) and IL-33, which belong to distinct cytokine families, induce and promote T helper type 2 airway inflammation. Both cytokines probably play a role in asthma, but there is a lack of direct evidence to clarify distinctions between their functions and how they might contribute to distinct 'endotypes' of disease. To address this, we made a direct comparison of the effects of IL-25 and IL-33 on airway inflammation and physiology in our established murine asthma surrogate, which involves per-nasal, direct airway challenge. Intranasal challenge with IL-33 or IL-25 induced inflammatory cellular infiltration, collagen deposition, airway smooth muscle hypertrophy, angiogenesis and airway hyperresponsiveness, but neither increased systemic production of IgE or IgG1. Compared with that of IL-25, the IL-33-induced response was characterized by more sustained laying down of extracellular matrix protein, neoangiogenesis, T helper type 2 cytokine expression and elevation of tissue damping. Hence, both IL-25 and IL-33 may contribute significantly and independently to asthma 'endotypes' when considering molecular targets for the treatment of human disease.

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Section: Methodsmentioning

confidence: 99%

“…It has also been implicated in the promotion of Th2 immune responses. Murine airways challenged directly with IL‐25 develop epithelial cell hyperplasia, mucous hypertrophy and hyper‐reactivity . Production of IL‐25 is also elevated in human asthma …”

Section: Introductionmentioning

confidence: 99%

Distinct sustained structural and functional effects of interleukin‐33 and interleukin‐25 on the airways in a murine asthma surrogate

Wang

Huang

et al. 2015

Immunology

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“…Mice were divided into 3 groups, including a group serially challenged with OVA (a "classical" allergen-induced asthma model) [14,17], a group challenged with saline as a negative control and a group serially challenged with IL-25. Briefly, OVA-challenged group were first sensitized by intraperitoneal injection of OVA (SigmaAldrich, Beijing, China, 100 μg emulsionised in Al[OH] 3/dose) on days 0 and 12.…”

Section: Allergen-and Il-25 Intranasal Instillation Protocolmentioning

confidence: 99%

“…The primary monoclonal antibody against mouse Von Willebrand factor (vWF, 1:50) was purchased from CHEMICON International, Inc. MA 01730. The PAP (peroxidase anti-peroxidase) technique was used as previously described [13][14][15]. Positively staining cells were detected using the glucose oxidase-DAB-nickel method [19].…”

Section: Lung Immunohistochemistrymentioning

confidence: 99%

IL-25 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma model

Yao¹,

Wang²,

Huang³

et al. 2015

5.3 Allergy and Immunology

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Background: Th2-promoting cytokine IL-25 might contribute to bronchial mucosal vascular remodelling in asthma through its receptor expressed by vascular endothelial and vascular smooth muscle cells. Methods: By utilising a newly established chronic asthma murine model induced by direct exposure of the airways to IL-25 alone, we examined effects of IL-25 on angiogenesis, vascular remodelling and expression of angiogenic factors, compared changes with those in a "classical" ovalbumin (OVA)-induced murine asthma model. IL-25 and OVA were intranasally instilled into the airways of BALB/c mice for up to 55 days. Airways vessels and angiogenic factors, including Von Willebrand Factor (vWF), amphiregulin, angiogenin, endothelin-1, transcription factor ERG, basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), insulin-like growth factor (IGF-1) and vascular endothelial growth factor (VEGF) in lung sections, homogenates and BAL fluid were detected and quantified by immunostaining or enzyme linked immunosorbent assay (ELISA). An in house assay was also utilised to compare the effects of IL-25 and other Th2-cytokines on angiogenesis by human vascular endothelial cells. Results: Repetitive intranasal challenge with IL-25 alone or OVA alone in OVA-presensitised animals significantly increased peribronchial vWF + vessels in the murine airways, which was associated with remarkably elevated expression of amphiregulin, angiogenin, endothelin-1, bFGF, EGF, IGF-1, VEGF and ERG. IL-25, but not Th-2-cytokines induced human angiogenesis in vitro. Conclusions: The data suggest that chronic exposure of murine airways to IL-25 alone is able to reproduce a local angiogenic milieu. Thus, blocking IL-25 may attenuate vascular remodelling and improve outcomes in asthma patients.

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“…Na asma, o dano ao epitélio fornece amplo suporte para a formação da resposta alérgica inflamatória Th 2 através da liberação de padrões moleculares associados ao dano (PMAD), linfopoetina estromal tímica (LPET), IL-25 e IL-33 (GREGORY et al, 2013;YAO et al, 2014). O surgimento das células linfoides inatas do tipo 2 (CLI2s), estruturalmente semelhantes aos linfócitos mas sem os marcadores característicos, são capazes de produzir grandes quantidades de IL-5 e IL-13 e promover uma inflamação em camundongos deficientes em linfócitos T e B (HENDRIKS, 2014).…”

Section: Il-33 E Sua Interação Com O Perfil Thunclassified

Novas Perspectivas Acerca do Contexto Inflamatório Th2 Na Asma

Souza

Silva

2015

SaudPesq

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RESUMO:A asma é responsável por acometer cerca de 300 milhões de pessoas por ano, resultando na sobrecarga dos sistemas de saúde e cofres públicos. Novas perspectivas em relação à função das células inflamatórias e citocinas envolvidas na resposta imune alérgica têm sido propostas. Nesta revisão buscou-se publicações científicas estrangeiras, escritas em língua inglesa, através da ferramenta de pesquisa da MEDLINE/PubMed, realizada nos meses de maio a julho de 2014. Descobertas recentes em relação ao papel dos mastócitos, células musculares lisas das vias aéreas, eosinófilos e citocinas do perfil Th 2 foram apontadas . Mastócitos estão mais ativos nas vias aéreas de pacientes com asma grave, podem ser ativados por uma via alternativa à clássica ligação cruzada com IgE e ainda podem induzir a polarização de células T. As células musculares lisas das vias aéreas atuam como fonte de citocinas e quimiocinas auxiliando na sinalização/recrutamento do processo inflamatório. Eosinófilos são células protagonistas na asma e podem ser recrutados por diferentes classes de eotaxina. A IL-33 vem sendo relacionada com as fases iniciais da inflamação, auxiliando na construção da resposta imune, por estimular a liberação de IL-5 e IL13, atuando no recrutamento e sinalização celular. Considera-se, portanto, que novos estudos precisam ser realizados com o objetivo de encontrar novos conhecimentos em relação a estas perspectivas, visando identificar novas alternativas para o tratamento da asma. Further studies are required to deepen information on these perspectives to identify new alternatives for the treatment of asthma. PALAVRAS-ChAVE

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Direct comparison of the dynamics of IL‐25‐ and ‘allergen’‐induced airways inflammation, remodelling and hypersensitivity in a murine asthma model

Cited by 38 publications

References 42 publications

Distinct sustained structural and functional effects of interleukin‐33 and interleukin‐25 on the airways in a murine asthma surrogate

Distinct sustained structural and functional effects of interleukin‐33 and interleukin‐25 on the airways in a murine asthma surrogate

IL-25 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma model

Novas Perspectivas Acerca do Contexto Inflamatório Th2 Na Asma

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